The proposed project will determine the neuroimmune interaction in the spontaneously hypertensive rat (SHR) which possesses an immune deficiency and an increased sympathetic activity. Stress and sympathetic activity are potentially important modulators of the immune system and can lead to decreased immunologic competence. Immune incompetence or deficiency is an important medical problem seen in both AIDS patients and those immunosuppressed because of organ transplants. In AIDS patients, stress is a contributing factor in reducing the latency period of the HIV virus. Through a better understanding of neural regulation of the immune system, it may be possible to increase the health of the general population and also help AIDS patients by increasing the latency period and decrease the severity of the symptoms. The SHR may prove a valuable model for these purposes, once its immune deficit and sympathetic innervation of immune organs are better characterized. The aims of the proposed project are: 1) to characterize the immune deficiency of the SHR compared to the Wistar Kyoto (WKY) rat by examining; lymphocyte subsets, ability to generate specific antibodies, ability to react to foreign cells, bioactivity of the T-lymphocyte growth factor Interleukin-2 and examine spleen and thymic sizes / histology. 2) To characterize the sympathetic innervation of thymus and spleen in SHR and WKY rats using histochemical, immunohistochemical and radioenzymatic assay methods. 3) To determine if there is a causal relationship between the sympathetic innervation and immune deficiency in the SHR, by examining the effect of immunosympathectomy on the SHR immune function. For this evaluation, immune function and splenic/thymic sizes and histology will be examined. The SHR model may prove to be valuable for both: a) understanding neurally induced immunodeficiency and b) testing drug efficacy for increasing immune function in the immune deficient subject (i.e. AIDS patients).